University Journal of Medicine and Medical Sciences

ISSN 2455- 2852 Volume 2 Issue 7 2016

AN INTERESTING CASE OF FEVER WITH CENTRAL CYANOSIS

MURUGA BHARATHY KALIMUTHU Department of General Medicine, MADRAS MEDICAL COLLEGE AND GOVERNMENT GENERAL HOSPITAL

Abstract : A 13 year old girl was admitted with a his- A 13 years old female presented with tory of fever for 10 days, which was high fever for 10 days with central cyanosis, grade intermittent associated with chills which did not improve with supplemental and rigors, with generalised body pain with oxygen, with no clinical evidence of res- no other positive history. She had been piratory or cardiac disorder. Pulse oxi- treated in a private hospital for the same metry showed spO2 of 82 percent and with chloroquine for 3 day, primaquine 15 arterial blood gas analysis showed PaO2 mg single dose, ceftriaxone 1gm for 3 days and SaO2 in the normal range. Echocar- with paracetomol 500mg 8th hourly for 5 diography and CT chest were normal. All days. On examination patient was fully other tests including tests for hemolysis conscious and oriented and she had fever were within normal limits. As there was of 100 ° F, with central cyanosis, no club- saturation gap, blood methemoglobin bing, no pallor, not jaundiced, no significant was tested. Methemoglobin level was 11 lymphadenopathy. Respiratory rate was percent on the second day of admission, 20/min, pulse rate was 130 / min. normo- which decreased to normal values in 8 volemic, had normal blood pressure. Oxy- days.G6PD levels within normal limits. gen saturation was 82% in room air. Chest Patient had been treated with chloro- was clear, heart sounds were normal, no quine for 3 days before she was referred organomegaly. to us. Fever subsided on the second day with symptomatic treatment. So we re- port this case, a case of acquired methe- moglobinemia due to chloroquine, a rare complication. Keyword : ,saturation gap, chloroquine.

CASE REPORT:

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complete hemogram, RFT and LFT re- mained normal. Blood methemoglobin th th levels on 4 and 7 day were 8% and 5% respectively. Patient made steady progress from 3rd day onwards and th was discharged on 8 day. DISCUSSION: CYANOSIS:

Bluish discolouration of skin and mu- cous membranedue to increased quan- 1 tity of 1) reduced >4g/dl 2) methemoglobin>1.5g/dl 3) sulfhemoglo- bin>0.5g/dl 4) abnormal hemoglobin It is PHOTOGRAPH SHOWING CHOCOLATE the ABSOLUTE, rather than the relative BROWN COLOUR BLOOD OF PATIENT amount of reduced hemoglobin that is ALONG WITH THE CONTROL important in producing cyanosis Site: PHOTOGRAPH SHOWING CENTRAL CYA- Mainly over lips, nail bed, ear and malar NOSIS IN THE PATIENT eminences. Diagnosed reliably when She was given inhaled oxygen, IV Ceftri- SaO2 <85%, and in dark skinned indi- axone, T.paracetomol and IV fluids. Investi- viduals when SaO2 < 75% Causes of gations showed Hb-10g%, WBC - 12,800 central cyanosis1: (neutrophils- 58%) and platelets -1.79 lacs. A. Decreased arterial oxygen saturation Blood urea and creatinine were normal. B. Hemoglobin abnormalities Urine routine was normal. Peripheral smear cDecreased arterial oxygen saturation showed microcytic hypochromic with 1 Decreased atmospheric pressure - of 2%. G6PD activity was nor- high altitude mal. Serum LDH was within normal limits. 2) Impaired pulmonary function Blood gas analysis showed partial pressure i. alveolar hypoventilation of oxygen 96 mm Hg with calculated SaO2 ii. ventilation-perfusion mismatch 94%. Smear for malaria and malaria antigen iii. impaired oxygen diffusion test were negative. Ultra sonogram ofabdo- 3) Anatomic shunt men revealed no significant findings. Blood 4) Hemoglobin with low affinity for oxy- cultures showed no growth. MSAT for lepto- gen spirosis and dengue IgM were negative. As B) Hemoglobin abnormalities patient’s cyanosis did not improve with sup- i. methemoglobin plemental oxygen, echocardiography and CT ii. sulfhemoglobin chest were done to rule out cardiac and res- Oxidant exposure is generally the cause piratory disorders, which were normal. As pa- of acquired methemoglobinemia as tient had saturation gap (difference between seen in exposure to drugs, chemicals or calculated SaO2 and pulse oximetry values), solvents6 or indirectly as in sepsis6,7,8,9. we thought of abnormal haemoglobin in By oxidation the ferrous molecule in the blood.Methemoglobin level estimation was hemoglobin gets oxidized to ferric form, sent on 2nd after admission. It was found to the resultant molecule is methemoglo- be raised to 12%, confirming the diagnosis of bin, which is incapable of binding oxy- methemoglobinemia. We added oral Ascor- gen. Usually levels greater than 2% are bic acid to the treatment. She became afeb- non physiological or abnormal. rile on 3rd day of admission and LDH,

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Symptoms generally appear when levels ex- The maximum dosage is 7mg/kg in 13,14,15 ceed 15% and levels >70 % may cause death. a 24-hour period . Spectral properties of methemoglobin are dif- ferent and it interferes with pulse oximetry A continuous infusion (0.1 mg/kg/ readings which are characteristically low. Arte- hr) may be considered in cases of rial blood gas partial pressures are very high agents (such as dapsone)that gen- because of high flow oxygen therapy. This erate methemoglobin over a long 16,17 case illustrates an uncommon condition i.e. period of time . methemoglobinemia precipitated by a very commonly used drug, Chloroquine. Chloro- Methylene blue causes the skin quine is a very widely used drug in India. and mucous membranes to have a Chloroquine induced methemoglobinemia has dusky-blue appearance.This can been reported before11. One should have a make the patient appear more cya- high index of suspicion and low threshold for notic and interfere further with investigations where cases are complicated. In pulse oximetry readings 18,19 the periphery, where investigation facilities are limited and even simple monitoring facilities • Possible causes of methylene like pulse oximetry are unavailable, early refer- blue treatment failure ral to higher centers in the event of complica- tions is recommended. • Concomitant severe hypoxemia

• Continued drug/toxin absorp- Management of methemoglobinemia: tion due to inadequate decontami- Methylene blue is the preferred antidote for nation 2,12 treatment of methemoglobinemia . it should be considered for use in sympto- • Discoloration of skin due to matic patients with methemoglobin levels large dose of methylene blue >20%, orasymptomatic patients with • Overwhelming and profound methemoglobin>30%.Patients who are oxidative stress from toxin or in- symptomatic or have concomitant medical gestion issues that compromise oxygendelivery to

tissues (e.g., anemia, carbon monoxide • exposure, cardiac disease, lung disease) should be treated with antidote at lower Unrecognized hereditary disorders: levels of methemoglobinemia if clinically Glucose-6-phosphate dehydro- indicated. genase (G6PD) deficiency,NAPDH • Methylene blue should be diluted to a 1% methemoglobinreductase defi- solution (10 mg/mL) and dosed as 1-2 mg/ ciency, presence of Hemoglobin M kgintravenously over 3-5 minutes. Vitamin C can be used in the treat- ment of familial idiopathic methe- • Clinical improvement is expected within moglobinemia 15 to 60 minutes. If minimal or no improve- ment isnoted at 30 minutes, a repeat dose of 1 mg/kg should be administered intrave- nously.

An Initiative of The Tamil Nadu Dr. M.G.R. Medical University University Journal of Medicine and Medical Sciences

CONCLUSION: 8 Ohashi K, Yukioka H, Hayashi M, Central cyanosis, needs prompt attention Asada A.: Elevated methemoglo- management. Respiratory and cardiovascu- binin patients with . Acta An- lar causes are to be sought in emergency aesthesiologica Scandinvica, 1998; department. A careful drug history and a 42:713-716. high index of suspicion are required for diag- nosis of abnormal , so that early 9 Rehman H U.: Methemoglobine- appropriate therapy can be instituted, espe- mia. The WesternJournal of Medi- cially for toxin induced methemoglobinemia cine, 2001;175: 193-196.

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7 Mansourie A, Lurie AA.: Concise re- 15 Berlin G, Brodin B, Hilden JO, view:methemoglobinemia. American Martenson J. Acute dapsone intoxi- Journal Hematology, 1993; 42:7–12. cation: a case treated with continu- ous infusion of methylene blue, forced diuresis and plasma ex- change. J toxicolclintoxicol .1985;22 (6):537-548.

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16 Dawson AH; Whyte IM. Management of dapsone poisoning complicated by methemoglobinemia. Med toxicol ad- verse drug exp.1989; 4(5):387-392.

17 Larsen VH, Freudendal-Pedersen, Fogh-Andersen N. The influence of pat- ent methylene blue on pulseoximetry and hemoximetry. Actaanaesthesiolscand suppl. 1995; 107:53-55.

18 Zablocki A et al; false indication of arterial oxygen desaturation and methe- moglobinemia following injection of me- thylene blue in urological surgery. Mil Med 1990; 155; 260.

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